Methanol Unit Converter

Methanol Unit Converter

Convert methanol between mg/dL, mg/L and mmol/L — and read the result knowing that methanol itself is not what blinds people. Formic acid is, so a falling level in an acidotic patient is the worst result on the page, not the best.

Methanol converter

Mass ⇄ molar
Enter the concentration as your laboratory reported it. Most hospitals cannot measure methanol quickly, and nothing on this page should be waited for: the antidote is started on suspicion, on acidosis or on a raised osmolal gap.
Two published thresholds, named rather than blended. The American Academy of Clinical Toxicology guideline treats a documented methanol above 20 mg/dL as an indication for an alcohol-dehydrogenase blocker — but its other two limbs matter more in practice, because they do not need a level at all: a history or strong suspicion of ingestion plus any two of arterial pH below 7.3, bicarbonate below 20 mmol/L and an osmolal gap above 10. The EXTRIP workgroup sets extracorporeal treatment above 700 mg/L (70 mg/dL) when fomepizole is running, 600 mg/L on ethanol and 500 mg/L with no blocker — and recommends it irrespective of the level for coma, seizures, new visual deficits, pH at or below 7.15, persistent acidosis or an anion gap above 24 mmol/L.
7.80mmol/LExample

Serum methanol reported as 25 mg/dL, read against the antidote threshold

The conversion, and the molecule that matters

mmol/L = mg/dL × 0.31211
mg/dL = mmol/L ÷ 0.31211
because 0.31211 = 0.01 g/L ÷ 32.04 g/mol, the molecular weight of methanol
MW 32.04
methanol, CH₃OH — the smallest alcohol, and the reason it raises the osmolal gap so much per milligram: a low molecular weight means many particles per unit mass
mg/dL and mg/L
1 mg/dL = 10 mg/L. North American and most toxicology reports use mg/dL; the EXTRIP recommendations are published in mg/L, so 700 mg/L is 70 mg/dL
formic acid
the actual toxin. Alcohol dehydrogenase converts methanol to formaldehyde and aldehyde dehydrogenase converts that to formate, which inhibits cytochrome c oxidase, poisons the optic nerve and generates the high anion gap acidosis. Methanol itself is little more intoxicating than ethanol
the latent period
typically 12 to 24 hours, and longer if ethanol was taken at the same time, because ethanol competes for the same enzyme. A well-looking patient at four hours is entirely compatible with blindness at twenty

Worked example

Serum methanol reported as 25 mg/dL, read against the antidote threshold
25 mg/dL = 250 mg/L — the same concentration written the other way
25 × 0.31211 = 7.80 mmol/L
The AACT antidote threshold of 20 mg/dL is 6.24 mmol/L, so 7.80 mmol/L is above it
The EXTRIP haemodialysis threshold on fomepizole is 700 mg/L — 70 mg/dL, or 21.85 mmol/L — so this concentration alone would not mandate dialysis, though coma, seizures, new visual loss, a pH at or below 7.15 or an anion gap above 24 mmol/L would, whatever the level says
Now the part the arithmetic cannot do. If this sample was taken 24 hours after the ingestion in a patient with a bicarbonate of 8 mmol/L, a methanol of 25 mg/dL is the tail of a much larger exposure that has already been converted to formate. The low-looking number and the dangerous patient are the same patient
And if the history is suggestive, the antidote goes in before any of this returns

Thresholds as published, in both units

Thresholdmg/dLmg/Lmmol/L
AACT — start an alcohol-dehydrogenase blocker (or on suspicion plus acidosis or osmolal gap)202006.24
EXTRIP — haemodialysis, no blocker given5050015.61
EXTRIP — haemodialysis, on ethanol6060018.73
EXTRIP — haemodialysis, on fomepizole7070021.85
Fomepizole may be stopped (label)under 20, patient asymptomatic with a normal pHunder 200under 6.24
The EXTRIP figures are published in mg/L and are reproduced here as they were written. Note that every one of these is a sufficient reason to act and none of them is a necessary one: EXTRIP also recommends extracorporeal treatment for coma, seizures, new visual deficits, a blood pH at or below 7.15, persistent acidosis or an anion gap above 24 mmol/L, whatever the concentration — and most hospitals cannot measure methanol at all out of hours.

The osmolal gap and the anion gap move in opposite directions

Time since ingestionMethanol levelOsmolal gapAnion gapWhat it looks like
Early (0–6 h)HighRaisedNormalA well or mildly drunk patient with a startling osmolal gap and normal chemistry
IntermediateFallingFallingRisingThe crossover — both gaps may be only modestly abnormal at once
Late (12–24 h+)Low or undetectableNormalWideSevere metabolic acidosis, visual loss, and a reassuring-looking methanol level
This is the single most dangerous pattern in toxic alcohol poisoning: the two tests that might have made the diagnosis are each normal at the time the other is abnormal. A normal osmolal gap at late presentation does not exclude methanol poisoning, and a low methanol level in an acidotic patient is a reason for more concern, not less. The <a href="/medical-laboratory-calculators/osmolal-gap-calculator/">osmolal gap calculator</a> and the <a href="/medical-laboratory-calculators/toxic-alcohol-level-from-osmolal-gap-calculator/">toxic alcohol level from osmolal gap calculator</a> cover the early half of this picture.

What each treatment does, and what it cannot do

TreatmentWhat it doesWhat it does not do
Fomepizole (or ethanol)Competitively inhibits alcohol dehydrogenase, so no further formaldehyde or formate is madeDoes nothing about formate already formed — the patient can continue to deteriorate on a perfectly blocked enzyme
HaemodialysisRemoves methanol and, importantly, formate; corrects the acidosisRequires a dialysis service, vascular access and time; it does not prevent injury that has already happened
Folinic acid (or folic acid)Accelerates the metabolism of formate to carbon dioxide and waterIs not a substitute for either of the above
Sodium bicarbonateCorrects acidaemia and shifts formate towards the ionised form, which crosses into tissue less readilyDoes not stop production and does not remove formate
The order matters. Blocking the enzyme early is what prevents injury, which is why the antidote is given on suspicion rather than on a level. Everything else is repair work. The <a href="/medical-laboratory-calculators/fomepizole-dose-calculator/">fomepizole dose calculator</a> sets out the schedule, including why the frequency increases during haemodialysis.

Why the level falls as the patient gets worse

Methanol is reported in milligrams per decilitre, or in milligrams per litre, or in millimoles per litre. The molecular weight is 32.04, so one milligram per decilitre is 0.31211 millimoles per litre, and the 20 mg/dL that appears in every guideline is 6.24 mmol/L. That is the whole of the arithmetic, and it is the least important thing on this page.

Methanol is not, in any meaningful sense, the poison. Swallowed methanol is mildly intoxicating and otherwise fairly inert; it becomes dangerous only when alcohol dehydrogenase oxidises it to formaldehyde and aldehyde dehydrogenase oxidises that to formic acid. Formate inhibits cytochrome c oxidase, injures the optic nerve and retina, and drives a wide anion gap metabolic acidosis that in turn makes formate cross into tissue more readily. Everything that makes methanol poisoning lethal — the acidosis, the basal ganglia injury, the blindness — is metabolite work. The parent alcohol is only the raw material.

That has a consequence which catches people out, and it is the reason this page exists. A low or falling methanol concentration is not reassurance in an acidotic patient. It may simply mean that the conversion has already happened, and that the formate is now where the methanol used to be. The same logic runs through the two gaps. Early, when the methanol is still methanol, it adds osmotically active particles and the osmolal gap is raised while the anion gap is normal; late, when it has become formate, the osmolal gap closes and the anion gap opens. A patient presenting a day after drinking may therefore have a normal osmolal gap, a nearly undetectable methanol level and be going blind. A normal osmolal gap does not exclude methanol poisoning, and neither does a low level.

Which is why nobody waits. The American Academy of Clinical Toxicology’s guideline lists a methanol concentration above 20 mg/dL as one indication for blocking alcohol dehydrogenase, but its other two limbs require no concentration at all: a history or strong suspicion of ingestion together with any two of an arterial pH below 7.3, a bicarbonate below 20 mmol/L and an osmolal gap above 10. Most hospitals cannot measure methanol at all, and those that can rarely do so within the window in which the antidote changes the outcome. Fomepizole, or ethanol where fomepizole is unavailable, is started on clinical suspicion — and because it only stops further formate being made, it is given as early as possible and combined with haemodialysis, which removes what has already been formed, and with folinic acid, which helps clear it. The level, when it eventually arrives, refines a decision that has already been made clinically. It does not make it.

Frequently asked questions

How do you convert methanol from mg/dL to mmol/L?

Multiply by 0.31211, which is 0.01 g/L divided by methanol’s molecular weight of 32.04 g/mol. So 20 mg/dL is 6.24 mmol/L and 70 mg/dL is 21.85 mmol/L. Divide by the same factor to go back. Note that 1 mg/dL is 10 mg/L, which matters because the EXTRIP dialysis recommendations are published in mg/L: their 700 mg/L threshold is 70 mg/dL.

What methanol level needs treatment?

The American Academy of Clinical Toxicology guideline gives 20 mg/dL (6.24 mmol/L) as one indication for an alcohol-dehydrogenase blocker, but the guideline’s other limbs deliberately do not need a level: a history or strong suspicion of ingestion plus any two of arterial pH below 7.3, bicarbonate below 20 mmol/L and an osmolal gap above 10. In practice the antidote is started on suspicion, because most laboratories cannot return a methanol concentration quickly enough for it to be the trigger.

Why is a low methanol level not reassuring?

Because methanol itself is not the poison. It is metabolised to formic acid, and formate causes the acidosis and the visual loss. A level that is low because the ingestion was small and a level that is low because the methanol has already been converted look identical on the report. The way to tell them apart is the acid-base picture: a low methanol with a wide anion gap acidosis is a late, dangerous presentation, not a mild one.

Does a normal osmolal gap exclude methanol poisoning?

No, and relying on it has cost people their sight. The osmolal gap is raised only while unmetabolised methanol is still circulating; once it has been converted to formate the gap closes and the anion gap widens instead. A patient presenting twelve to twenty-four hours after ingestion can have a normal osmolal gap and severe poisoning. The osmolal gap is also insensitive because the normal range is wide, so a gap within it can still conceal a clinically important concentration.

What does fomepizole actually do to a methanol level?

It stops the level falling, which is the point. Fomepizole competitively inhibits alcohol dehydrogenase, so methanol is no longer converted to formaldehyde and formate; the methanol then clears slowly by renal and pulmonary routes, with an elimination half-life of many hours. A persistently high methanol on fomepizole is evidence the block is working, not that treatment is failing. Removing the methanol and the formate that has already been made is what haemodialysis is for.

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References

  1. Barceloux DG, Bond GR, Krenzelok EP, Cooper H, Vale JA; American Academy of Clinical Toxicology Ad Hoc Committee on the Treatment Guidelines for Methanol Poisoning. American Academy of Clinical Toxicology practice guidelines on the treatment of methanol poisoning. J Toxicol Clin Toxicol. 2002;40(4):415–446.
  2. Roberts DM, Yates C, Megarbane B, et al; EXTRIP Work Group. Recommendations for the role of extracorporeal treatments in the management of acute methanol poisoning: a systematic review and consensus statement. Crit Care Med. 2015;43(2):461–472. Extracorporeal treatment recommended for coma, seizures, new visual deficits, blood pH at or below 7.15, persistent metabolic acidosis, anion gap above 24 mmol/L, or serum methanol above 700 mg/L on fomepizole, 600 mg/L on ethanol, 500 mg/L with no blocker.
  3. Brent J, McMartin K, Phillips S, Aaron C, Kulig K; Methylpyrazole for Toxic Alcohols Study Group. Fomepizole for the treatment of methanol poisoning. N Engl J Med. 2001;344(6):424–429.
  4. Kraut JA, Mullins ME. Toxic alcohols. N Engl J Med. 2018;378(3):270–280.
  5. Fomepizole injection, USP — prescribing information. DailyMed, US National Library of Medicine. Treatment may be discontinued when ethylene glycol or methanol concentrations are undetectable or reduced below 20 mg/dL and the patient is asymptomatic with a normal pH.

Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.